The broad immunopathologic spectrum of leprosy ranging from strong manifestations of cellular immunity at the tuberculoid pole and humoral antibody manifestations at the lepromatous pole provides a single pathogen/single host model for the study of macrophage deficiency at the lepromatous pole. Elucidation of these functional and possible enzymatic deficiencies in contrast to the effectiveness of cellular immunity at the tuberculoid pole provides a model for enhanced understanding of the relationships between cellular immunity and cell enzymology.